ArticleAmerican journal of human genetics2000
The use of case-parent triads to study joint effects of genotype and exposure.
Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
65 citing papers in PubMed.
- Estimation of direct and indirect polygenic effects and gene-environment interactions using polygenic scores in case-parent trio studies.Nature genetics · 2026Article
- Genome-Wide Association Analyses in Family Triads and Dyads Following Assisted Reproductive Technology.Genetic epidemiology · 2025Article
- Estimation of Direct and Indirect Polygenic Effects and Gene-Environment Interactions using Polygenic Scores in Case-Parent Trio Studies.medRxiv : the preprint server for health sciences · 2025Article
- Foetal haemoglobin elevation, unfavourable prognosis, and protective role of genetic variantsJournal of genetics · 2024Article
- Maternal Transmission of theGlobal medical genetics · 2023Article
- Gene-methylation interactions: discovering region-wise DNA methylation levels that modify SNP-associated disease risk.Clinical epigenetics · 2020Article
- Identification of germline and somatic mutations in pancreatic adenosquamous carcinoma using whole exome sequencing.Cancer biomarkers : section A of Disease markers · 2020Article
- Exome sequencing of family trios from the National Birth Defects Prevention Study: Tapping into a rich resource of genetic and environmental data.Birth defects research · 2019Article
- Neuroblastoma in relation to joint effects of vitamin A and maternal and offspring variants in vitamin A-related genes: A report of the Children's Oncology Group.Cancer epidemiology · 2019Article
- Haplin power analysis: a software module for power and sample size calculations in genetic association analyses of family triads and unrelated controls.BMC bioinformatics · 2019Article
- PDGFRA gene, maternal binge drinking and obstructive heart defects.Scientific reports · 2018Article
- Using imputed genotype data in the joint score tests for genetic association and gene-environment interactions in case-control studies.Genetic epidemiology · 2018Article
- The Gene Variants of Maternal/Fetal Renin-Angiotensin System in Preeclampsia: A Hybrid Case-Parent/Mother-Control Study.Scientific reports · 2017Article
- Maternal gene-micronutrient interactions related to one-carbon metabolism and the risk of myelomeningocele among offspring.Birth defects research · 2017Article
- A family-based study of gene variants and maternal folate and choline in neuroblastoma: a report from the Children's Oncology Group.Cancer causes & control : CCC · 2016Article
- Gene-environment interaction between the oxytocin receptor (OXTR) gene and parenting behaviour on children's theory of mind.Social cognitive and affective neuroscience · 2015Article
- Detecting gene-environment interactions in human birth defects: Study designs and statistical methods.Birth defects research. Part A, Clinical and molecular teratology · 2015Article
- Disentangling pooled triad genotypes for association studies.Annals of human genetics · 2014Article
- Detecting maternal-fetal genotype interactions associated with conotruncal heart defects: a haplotype-based analysis with penalized logistic regression.Genetic epidemiology · 2014Article
- Testing gene-environment interactions in family-based association studies using trait-based ascertained samples.Statistics in medicine · 2014Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Most noninfectious disease is caused by low-penetrance alleles interacting with other genes and environmental factors. Consider the simple setting where a diallelic autosomal candidate gene and a binary exposure together affect disease susceptibility. Suppose that one has genotyped affected probands and their parents and has determined each proband's exposure status. One proposed method for assessment of etiologic interaction of genotype and exposure, an extension of the transmission/disequilibrium test, tests for differences in transmission of the variant allele from heterozygous parents to exposed versus unexposed probands. We show that this test is not generally valid. An alternative approach compares the conditional genotype distribution of unexposed cases, given parental genotypes, versus that of exposed cases. This approach provides maximum-likelihood estimators for genetic relative-risk parameters and genotype-exposure-interaction parameters, as well as a likelihood-ratio test (LRT) of the no-interaction null hypothesis. We show how to apply this approach, using log-linear models. When a genotype-exposure association arises solely through incomplete mixing of subpopulations that differ in both exposure prevalence and allele frequency, the LRT remains valid. The LRT becomes invalid, however, if offspring genotypes do not follow Mendelian proportions in each parental mating type-for example, because of genotypic differences in survival-or if a genotype-exposure association reflects an influence of genotype on propensity for exposure-for example, through behavioral mechanisms. Because the needed assumptions likely hold in many situations, the likelihood-based approach should be broadly applicable for diseases in which probands commonly have living parents.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.